With an aging population, cost-effective patient management of chronic heart disease is a high priority for today's medical device industry. In particular, pacemaker companies are increasingly interested in adding sensors and monitors to their implantable devices. For example, the United States Food and Drug Administration (FDA), which regulates medical devices, recently approved an implantable defibrillator that uses measured impedance to monitor edema, a pathology associated with advanced heart failure. If a heart failure patient decompensates (meaning that normal fluid balance is lost as a result of poor ventricular function, causing fluid backup in the venous systems), edema may develop in the lungs and tissues. The device may provide advanced warnings, and therefore allow for opportune corrective interventions. Costly hospitalizations may thus be avoided.
It is known that the conventional twelve-lead electrocardiogram (ECG), externally recorded with skin electrodes attached externally to a patient's skin, displays variations when there are abnormalities of the left atrium, one of the four chambers of the heart. This ECG variation has been referred to as “left atrial abnormality,” or “left atrial enlargement.” Cardiology textbooks describe an association of this finding with enlargement of, or high blood pressures within, the left atrium, as well as with electrical conduction defects between the right atrium and the left atrium of the heart. Several studies have established the relation of the left atrial abnormality to edema and decompensation in heart failure.
One study investigated the relationship between lung edema clearance and the ECG variation, measured in the study using a quantity known as “PTF-V1,” which refers to the electrocardiographic force of the terminal P-wave, as monitored in lead V1. The electrocardiographic force is known to be estimated by multiplying the duration of the ECG wave in question by its amplitude. In the study, patients who were in pulmonary edema initially presented with ECG (PTF-V1) more negative than −0.03 mm-secs. When the patients were treated and their pulmonary edema relieved, the PTF-V1 magnitude on the ECG dropped significantly. This finding provides motivation for using this variation of the ECG as a marker for edema. Later investigation established that the true mechanism for the ECG PTF-V1 finding is a condition known as inter-atrial block. This condition occurs when the activation of the left atrium lags abnormally in time with respect to the right atrium. The term “block” denotes an abnormal delay of the normal right to left conduction in the atria.
FIG. 1 shows conventional twelve-lead ECG traces 2, 4, externally recorded with conventional skin electrodes for a patient suffering from inter-atrial block. The Lead II trace 2 shows a widened P-wave 6 with a notch 8 at a location where a peak of the P-wave 6 should be, caused by an abnormally delayed activation of the left atrium with respect to the right atrium. This notch 8 is indicative of inter-atrial block, in contrast to a P-wave of a healthy patient, which would not include a significant notch. The Lead V1 trace 4 also shows a P-wave 10 that has a pronounced negative trough 12, indicative of inter-atrial block. This negative trough 12 develops in the second half of the P-wave, referred to as the terminal P-wave. Because of these ECG changes, this abnormality is also referred to as a rotation of the terminal part of the P-wave cardiac vector. The development of a larger negative voltage in lead V1 implies a more posterior and left direction of that cardiac vector.
Present medical knowledge contemplates that this inter-atrial block is secondary to fluid overload (as in thoracic edema) stressing the left atrium, either by enlarging it or straining it with high pressure. An enlarged left atrium also poses risks for atrial fibrillation, an undesirable cardiac arrhythmia, as well as an enhanced risk for dangerous blood clots (i.e., systemic embolisms).
Because a conventional ECG is administered by a physician at a medical facility, the patient must ordinarily schedule an appointment for the procedure and submit to the examination at the medical facility. Moreover, the conventional ECG captures an indication of cardiac activity over only a small, finite time interval. As such, a patient in the early stages of inter-atrial block may elude detection by conventional ECG monitoring techniques because the disease may progress following the initial examination. It would be desirable to periodically monitor for the inter-atrial block condition twenty-four hours a day. Patients with such a monitor could be warned of an impending edema decompensation, or of the appearance of an undesirable atrial fibrillation precursor.
One way to monitor for inter-atrial block is to measure the conduction time between the activation of the left atrium and the right atrium. This can be measured in a catheter lab, and can also be done using an implanted medical device, such as a pacemaker or defibrillator. FIG. 2a is a diagram of a human heart 30 with implanted electrodes and leads. Right atrium electrodes 32 are located in a right atrium 34 of the heart 30, coronary sinus electrodes 36 are located in a coronary sinus 38 (shown in dashed lines) of the heart 30, and coronary vein electrodes 40 are located in coronary veins over a left ventricle 42 of the heart 30. The right atrium electrodes 32 are attached to a right atrium lead 44, and the coronary sinus electrodes 36 and coronary vein electrodes 40 are attached to a left ventricular lead 46.
FIG. 2b is a view of a right atrium electrogram trace 50 and a left atrium electrogram trace 52. The right atrium electrogram trace 50 can be measured using the right atrium electrodes 32, and corresponds primarily to that portion of the electrical cardiac P-wave associated with the right atrium. As such, the right atrium electrogram trace 50 indicates when the right atrium activates. The left atrium electrogram trace 52 can be measured by the coronary sinus electrodes 36, and corresponds primarily to that portion of the P-wave associated with the left atrium, thus indicating when the left atrium activates. An inter-atrial delay 54 can be measured between common points of the right atrium electrogram trace 50 and the left atrium electrogram trace 52, and this delay 54 can be monitored over time. In FIG. 2b, the inter-atrial delay 54 is measured between peaks of the electrogram traces 50, 52.
However, using an implanted medical device to measure activation delays accurately requires a nonstandard lead arrangement, such as using a multipolar coronary sinus lead, which poses mechanical challenges (e.g., connectors, feed-throughs and attendant size and complexity that they introduce, along with concerns related to lead fatigue resistance and lead diameter). Requiring a multipolar coronary sinus lead may exclude patients receiving a device upgrade or replacement (due to battery exhaustion, for example). Additionally, adding electrodes to standard leads can be difficult because the industry may be resistant to change.